LncRNA PART1 alleviated myocardial ischemia/reperfusion injury via suppressing miR-503-5p/BIRC5 mediated mitochondrial apoptosis.

BACKGROUND

Long non-coding RNA (lncRNA) is crucial for heart development and for adult heart structural maintenance and function. Herein, we performed a study to explore the effect of lncRNA PART1 on myocardial ischemia-reperfusion (I/R) injury by targeting BIRC5 through miR-503-5p pathway.

METHODS

I/R model was created in vivo and vitro. The level of gene and protein was detected by RT-PCR and western blot. The apoptosis level was assessed by TUNEL and flow cytometry. Cell viability was determined by MTT. Mitochondrial function was evaluated by ATP content, ROS production, GSH level, and mitochondrial membrane potential. Cardiac function was confirmed by echocardiography, TTC staining, and H&E staining.

RESULTS

Here, we found that the expression of lncRNA PART1 was down-regulated in the I/R hearts and H/R cardiomyocytes. Forced expression of PART1 remitted cardiac I/RI and H/R cardiomyocyte injury. Silencing of PART1 aggravated apoptosis and mitochondrial damage in cardiomyocytes. We found that PART1 functioned as a competing endogenous RNA of miR-503-5p, which decreased the expression of miR-503-5p. We further established BIRC5 as a target of miR-503-5p. Furthermore, PART1 prevented apoptosis and improved mitochondrial function in myocardial I/RI by targeting miR-503-5p/BIRC5.

CONCLUSIONS

In summary, PART1 protected mitochondrial function via miR-503-5p/BIRC5 pathway in MI/RI, which may provide the new theoretical basis for MI/RI treatment in the clinic.